Ning Chang

The paper identifies BAZ1A as an epigenetic facilitator of DUX4 and DBE-T expression in FSHD, showing that inhibiting BAZ1A disrupts a feed-forward loop that promotes disease pathology.

This study identifies a compound, C06, that effectively represses DUX4 expression in FSHD myocytes using AI-based screening and validation.

The paper investigates the role of Dux and MERVL in ZGA, totipotency, and cell toxicity using CRISPRa and a 2C-GFP reporter system, finding that MERVL activation contributes to expanded fate potential but not all totipotency features, while Dux-induced toxicity is independent of MERVL and involves Noxa.